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Biomedical subjects

V Foà

Publications and source records attributed to V Foà.

At least 19 recordsLinked to original sources

Occupational triphenyltin acetate poisoning: a case report.

A case of triphenyltin acetate (TPTA) poisoning is described. The patient, who had been exposed mainly to cutaneous absorption, showed acute stages of an urticarial eruption, signs of hepatic injury, slight glucose intolerance, and electroencephalographic abnormalities. Concomitant with the highest concentrations of tin in plasma and the peak of tin excretion in urine, neutrophils did not show the normal increase in actin polymerisation after stimulation with a chemotactic peptide (100 nM fMLP). The peak of urinary excretion of tin occurred between the fifth and the sixth day after poisoning; subsequently, the rate of excretion became slow, suggesting biphasic kinetics with the possibility of a cumulative trend.

Adult

[Health risks in the biotechnological industry].

Biotechnology has been defined as the application of biological organisms, systems or processes to manufacturing and service industries. In considering health aspects of biotechnological development it must be underlined that the use of microorganisms in traditional industries, such as the production of food, bread, beer and dairy products, has not added significantly to the more usual industrial hazards. The risk factors encountered in the biotechnology industry can be defined as general, i.e., common to other industrial activities, and specific, i.e., depending on the presence of microorganisms and/or their metabolic products. The specific health risks vary according to the type of process, but can be grouped into three main categories: immunological diseases, toxic effects; pathological effects of microorganisms. Allergic immunological diseases such as bronchial asthma, contact dermatitis, oculo-rhinitis and extrinsic allergic alveolitis are by far the most frequent and well known diseases occurring among workers employed on biotechnological production. Toxic effects were observed among workers employed on the production of antibiotics and hormones or single cell proteins, where absorption of endotoxins has been described. Infectious diseases may arise from uncontrolled dissemination of pathogenic microorganisms through aerosols, dusts, aqueous and semisolid sludge effluents from biotechnological plants. The greatest risks occur in the production of antiviral vaccines, in research laboratories and in waste-water treatment plants. Risk of pathogenic effects has also been speculated from exposure to engineered microorganisms in laboratory and environmental or agricultural applications. Safety precautions consisting of protective measures, and effective barriers of containment (both physical and biological) have to be advised according to the hazardous characteristics of the organisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Biotechnology

[Creatinine as an adjustment parameter in urinary excretion of vanadium and nickel].

Urinary creatinine is used as an adjustment factor of the concentration of metabolites excreted in urinary random samples. The usefulness of this practice is longtime disputed. The aim of this study, made in 94 workers, is to estimate if the creatinine-adjustment of V and Ni urinary concentrations brings a true advantage in his capacity to predict the amount of metal excreted in 24 hours. The results shown this practice is pointless and that also in case of urinary samples at anomalous dilution. A greater accuracy in expression of analytical results of V and Ni excretion may be obtained collecting the urinary samples with a known amount, that is to say more representative of the daily diuresis.

Adult

A cohort study on vinyl chloride manufacturers in Italy: study design and preliminary results.

A cohort mortality study of 5000 vinyl chloride manufacturers is ongoing in 9 Italian plants. They represent the entire workforce of those ever employed in the production of the monomer and its polymerization. The objectives of the study are to investigate the mortality of the exposed population and to clear up the carcinogenic spectrum of vinyl chloride. This article gives the results for 3 out of 9 plants, Rosignano, Ferrara and Ravenna, which represent about 25% of the total cohort. The expected deaths have been calculated using the mortality rates of the Italian population. For the deceased persons information from the death certificates were used in the analysis of mortality; additional clinical and pathological data were collected (best pathological evidence, b.p.e.). In Ferrara a statistically significant excess for all malignant tumors and lung cancer was detected. In Rosignano and Ravenna the number of observed deaths were small and therefore no comments can be made on cancer mortality. The cohort study is ongoing in the 6 remaining cohorts and the future analysis will consider duration and level of exposure and latency.

Adult

The speciation of the chemical forms of arsenic in the biological monitoring of exposure to inorganic arsenic.

Total As content may be determined in blood and urine by means of an AAS method that involves reduction of As to its volatile hydride and ashing at 600 degrees C with MgO and Mg (NO3)2. Separation of inorganic As (InAs), monomethylarsonic acid (MMA) and dimethylarsinic acid (DMAA) by ion-exchange chromatography, followed by direct AAS analysis, allows the determination of each As species in the urine. In a reference population of 148 subjects with only normal environmental exposure to As, total As concentration in the urine averages 17.2 +/- 11.1 micrograms/l. Urinary As consists of 10% each of InAs, MMAA and DMAA, the remaining 70% consisting of other forms of organic As. Blood As concentration averages 5.1 +/- 6.9 micrograms/l and correlates significantly with the urinary concentration of InAs and the sum of its metabolites (InAs + MMAA + DMAA). Inorganic arsenic undergoes methylation in the organism. After ingestion of high quantities of As2O3, the time course of excretion of its metabolites indicates that As methylation occurs by a saturable mechanism. In workers exposed to As2O3, InAs, MMAA and DMAA are the only chemical forms of As excreted in the urine that are relevant to a study of occupational exposure. Blood As concentration is proportional to exposure and correlates only with urinary DMAA excretion; DMAA seems to be the most appropriate single indicator of exposure. At high levels of exposure (total As excretion above 200 micrograms/l), As accumulates in the organism and DMAA excretion reflects its accumulation. At low levels of exposure (total As excretion below 50 micrograms/l) a short-term accumulation does not occur and the best biological indicator of exposure is InAs excretion. Seafood ingestion brings about a marked increase in urinary excretion of total As that lasts for 24-48 h and is not accompanied by any increase in InAs, MMAA or DMAA excretion. Organic As from seafood does not mix with the pool of inorganic As in the organism and may be separately detected in urine. In the biological monitoring of human exposure to As, particularly in the case of high urinary values, the speciation of the chemical forms of As in urine is necessary in order to establish with certainty the source, industrial or alimentary, of exposure.

Arsenic

Significance of arsenic metabolic forms in urine. Part I: Chemical speciation.

The aim of this research has been to develop analytical procedures whereby the various chemical forms of arsenic present in urine can be distinguished and further data on the biotransformation of absorbed arsenic can be acquired. The separation of inorganic arsenic ( InAs ), monomethylarsonic acid ( MMAA ), and dimethylarsinic acid ( DMAA ) in urine was performed by ion-exchange chromatography on AG 50 W-X8 resin. Arsenic was then measured directly on the eluted fractions by atomic absorption spectrophotometry, after the reduction of arsenic to the correspondent arsine. In 160 subjects with no occupational exposure to arsenic compounds, InAs , MMAA , DMAA each accounted for about 10% of the total arsenic urinary excretion (17.2 +/- 11.1 micrograms/1), thus indicating that in the normal population over 60% of arsenic in urine is present in other organic forms. After eating marine food, there was a marked increase of urinary output of arsenic, but no increase was observed in InAs , MMAA and DMAA urinary excretion. In the biological monitoring of exposure to inorganic arsenic, particularly in the case of high urinary excretion values, the differentiation of the excreted forms of arsenic is necessary to establish with certainty the source (industrial or alimentary) of arsenic.

Adult

Low-pH method for the enzymatic assay of D-glucaric acid in urine.

The enzymatic methods for measuring D-glucaric acid in urine are based on the conversion of D-glucaric acid into its 1,4-lactone and measurement of inhibition of 1,4-lactone against beta-glucuronidase at pH 5.0. All the enzymatic methods described suffer from the disadvantage of a procedure that is complicated and inherently inaccurate, because the nature of glucaric acid/1,4-lactone equilibrium has not been properly considered in the development of such methods. After elucidating the factors influencing glucaric acid/1,4 lactone equilibrium in more detail, a low-pH enzymatic method has been developed in which the 1,4-lactone is formed in the urine sample by acid boiling at pH 3.8 and assayed at the same pH using beta-glucuronidase from Limpets. This procedure allows the acid/lactone equilibrium to remain stable during both the lactonization step and the enzymatic assay. The coefficient of variation for the proposed method (within-run and between-day precision) was from 4.2 to 8.7. The analytical recovery varied from 92-108%.

Glucaric Acid

Influence of sex, age, and smoking habits on the urinary excretion of D-glucaric acid.

Reference values for urinary D-glucaric acid and the influence of sex, age and smoking habits were evaluated with a low-pH enzymatic method. D-Glucaric acid measured on spot urine samples from 573 healthy subjects gave mean concentrations (mumol/1) and D-glucaric acid/creatinine ratios (mmol/mol creatinine) of 56.1 (+/- 22.9) and 3.05 (+/- 0.99) for males and 53.3 (+/- 20.9) and 3.35 (+/- 0.95) for females. No difference between morning and evening was observed for urinary D-glucaric acid/1 values, but D-glucaric acid/creatinine was higher in the evening samples for both sexes. There was a negative correlation between D-glucaric acid/1 values and age in males but not in females: the decrease of D-glucaric acid concentration was, however, quantitatively very small. Smoking produced a significant increase in D-glucaric acid concentration and in the D-glucaric acid/creatinine ratio for males and also partially for females.

Adolescent

Liquid chromatography of urinary porphyrins for the biological monitoring of occupational exposure to porphyrinogenic substances.

Very sensitive and precise analytical methods for measuring total porphyrin excretion and the relative amounts of different porphyrins in urine are required in order to monitor the biological effects of porphyrinogenic substances in workers and the general population. Many analytical steps of a HPLC method for measuring porphyrins as methyl esters in urine have been perfected. Sensitivity is 0.1 microgram/1 for each type of porphyrin, and average recovery is 92% in the range of 50-450 micrograms/liter porphyrins. The coefficient of variation is 3.4% within a series and 12.5% between series. Chemical oxidation before analysis and appropriate storing of the samples are the key points in achieving high quality results. The urinary excretion of porphyrins in healthy male workers varies within the range 21 to 161 micrograms/liter (95% limits of a group of 78 subjects). Concomitant factors, like drug use or liver disorders, were found to alter urinary porphyrin excretion. The proposed method permits the detection of extremely small alterations in porphyrin excretion resulting from occupational exposure to industrial chemicals such as, for example, mild coproporphyrinuria or early stages of chemical porphyria induced by polyhalogenated arylhydrocarbons.

Adult

Intracellular interaction and metabolic fate of arsenite in the rabbit.

Rabbits were treated with single doses of 50 micrograms AsO2-/kg b.w. by IP injection. At 48 h, 83.0 +/- 2.1% of arsenic is excreted via the urine. Also in blood the clearance of arsenic is rapid. Liver, kidney, and lung, among the tissues tested, show the highest concentration of arsenic at 5, 16, and 48 h after injection. Arsenic was found to be present at subcellular levels mainly in the nuclear and soluble fractions of the above-mentioned tissues. Chromatographic studies performed by gel filtration have shown that in plasma and in lung cytosol, arsenic is present, associated mainly to low molecular weight components, whereas in liver and kidney cytosol it is prevalently recovered in the fractions corresponding to the high molecular weight components. This different interaction of arsenic with molecular components was shown to influence the metabolic fate of this compound in the rabbit.

Animals

Carbon disulfide neuropathy in rats. A morphological and ultrastructural study of degeneration and regeneration.

The aim of this study was to elucidate the site and detailed nature of peripheral nerve damage induced in the rat by chronic CS2 inhalation exposure in the light of the relationship between pathological and neurophysiological data. Adult male rats were exposed to 700 ppm of CS2 2 h/d, 5 d/week for 12 weeks and then followed-up for 18 weeks. The first alteration observed was a decrease in the nerve conduction velocity, discovered after only 3 weeks of exposure. Pathological lesions were first observed in the 10th week and consisted of a typical "giant axon" axonopathy. Obvious pathological lesions of the myelin sheaths were revealed much later, in the 3rd week after the end of exposure, when some nerve fibers were dying back. Recovery took place with the regeneration of new fibers which started in the 8th week after the end of exposure and was nearly complete in the 18th week. These findings demonstrate that CS2-induced polyneuropathy is an axonopathy very similar to that caused by other occupational neurotoxic agents like MnBK, n-hexane, and acrylamide. The timing of the pathological events within the nerve fibers suggests that the pathogenesis of the nerve lesions should probably be attributed to a primary energy failure of the axonal membrane induced by CS2.

Animals

Effects of ganglioside therapy on experimental CS2 neuropathy.

Both in animals and in man the inhalation of CS2 vapor induces a chronic polyneuropathy with primary lesions in the axons of peripheral nerves. Since it was reported in several studies that the administration of gangliosides improves nerve regeneration and the functional recovery of nerves damaged by section as well as cryodegeneration, a study was undertaken to evaluate the effects of bovine-brain gangliosides administration on the experimental CS2 neuropathy in the rat. One hundred and fifty male rats were intoxicated with CS2 by a discontinuous inhalation exposure to 700 ppm for 12 weeks until a clear neuropathy developed. Thereafter the animals were subdivided at random into five groups and treated in different ways: 10 mg/kg BW gangliosides, 0.5 mg/kg gangliosides, 0.5 mg/kg vitamin B1, and 1 mg/kg vitamin B6, physiological solution, and controls without any treatment. The recovery from neuropathy was controlled for 18 weeks of treatment and assessed periodically by means of clinical, electromyographic, and morphological examination. The results of morphological studies showed more pronounced regeneration activity in the rats treated with the high dose of gangliosides than in all others, while no differences among the groups could be observed as far as clinical and neurophysiological parameters are concerned. The mechanism supporting this ganglioside-induced effect has so far not been ascertained, and further studies on this subject are in progress.

Animals